ArticleScientific reports2026
Repairing Atp10D in C57Bl/6J mice restores protein expression but does not mitigate metabolic stress from high fat diet.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
C57BL/6J mice are widely used in biomedical research and are susceptible to insulin resistance and dyslipidemia when challenged with high fat diets relative to other inbred strains. Interestingly, C57Bl/6J mice contain a naturally occurring premature termination codon in the lipid flippase Atp10D, and previous studies have linked Atp10D to the metabolic disease-prone phenotype in mice and atherosclerotic severity in humans. In this study, we used CRISPR/Cas9 to revert the premature termination codon to the wild-type glutamine codon (Atp10D *817Q) in the C57Bl/6J mouse strain. The RNA transcripts from original and corrected alleles are dually expressed in heterozygous mice, suggesting that the mutant transcript escapes nonsense-mediated decay. Expression of two corrected Atp10D alleles restores wildtype expression levels of the transcript and protein in the liver. When challenged with a high fat diet, Atp10D
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